Lightning strike is a rare natural phenomenon, which carries
a risk of dramatic medical complications to multiple organ systems and
a high risk of fatality. The known complications include but are
not limited to: myocardial infarction, arrhythmia, cardiac contusion,
stroke, cutaneous burns, respiratory disorders, neurological disorders,
acute kidney injury and death. We report a case of a healthy
young man who suffered a lightning injury and discuss the
cardiovascular complications of lightning injury, ranging from ECG
changes to death. The patient in our case, a 27-year old
previously healthy male, developed a syndrome of rhabdomyolysis and
symptomatic cardiogenic pulmonary edema. Electrocardiographic findings
included transient T-wave inversions, late transition shift and long
QT. His clinical condition improved with supportive measures.

Early recognition of lightning injury syndromes and anticipation of
complications may help us improve outcomes for these patients.
Evaluation of patients having experienced a lightning injury should
include a minimum of a detailed history and physical examination,
12-lead ECG and drawing of baseline troponins. Prolonged
electrocardiographical monitoring (for monitoring of ventricular
arrhythmias) and assessment for signs and symptoms of hemodynamic
compromise may be warranted.

Lightning strike is a rare natural phenomenon which carries a risk of
dramatic medical complications to multiple organ systems and a high
risk of fatality [1].The known complications include but are not
limited to: myocardial infarction, arrhythmia, cardiac contusion,
stroke, cutaneous burns, respiratory disorders, neurological disorders,
acute kidney injury and death.

We report a case of a young man struck by lightning and discuss the
cardiovascular complications of lightning injury.

Methods

Case report from our institution. Articles were selected from a
computerized literature search in the Medline database using the key
words: Lightning, Lightning Injuries, Electric Burns, Electric
Injuries, Cardiac Arrhythmias, Contusions, Heart Injuries, Thoracic
Injuries, Electrocardiography, Long QT, Myocardial Infarction,
Myocardial Ischemia, Cardiology and all the possible combinations of
the above. Two independent investigators (WFM, AB) reviewed the
abstracts and selected the ones considered of interest for the review.
Discrepancies were solved by consensus.

Case Report

A 27 year-old male presented to hospital the day after a lightning
strike complaining of nausea and vomiting, forearm pain, confusion,
decreased urine output and shortness of breath. He had no
recollection of the injury. His past medical history was significant
for infection with Hepatitis C virus, meningitis, cigarette smoking and
previous intravenous drug use. He had no pre-admission
medications. His physical examination was unremarkable, save for
2nd-degree burns on both forearms.

A 12-lead electrocardiogram (Figure 1)
showed sinus rhythm at 98 bpm, T-wave inversion in the precordial and
limb leads, late transition shift, rS pattern in leads I and aVL and
long QT interval (QTc= 500 ms).

Figure 1:
Twelve-lead electrocardiograms from a 27-year old male
struck by lightning. Panel A (Above): ECG recorded approximately 24
hours after
the event displaying diffuse T-wave inversion, late transition shift
and long QT interval (QTc= 500 ms). Panel B (Below): Follow-up ECG 5
days later
showing resolution of T-wave inversion in leads V1-V3, persistence of
late transition shift and a decrease in the QT interval to (QTc =
464
ms).

The patient's acute kidney injury was treated with intravenous fluid
and sodium bicarbonate administration. Urine output over the first 48
hours was 0.51 cc/kg/hr. On the 2nd post-admission day, the patient
became acutely short of breath. Chest radiographs were consistent with
pulmonary edema and the patient was treated symptomatically with
intravenous furosemide.

A 12-lead ECG recorded on the 5th post admission day had had begun to
normalize, displaying complete resolution of T-wave inversion in leads
V1-V3, persistence of late transition shift and a decrease in the QT
interval (QTc = 464 ms).The patient was discharged home on the 11th
post-admission day with a creatine of 142 mcmol/L, creatinine
phopshokinase of 0.131 U/L and potassium of 4.0 mmol/L and received no
outpatient cardiac medications.

Discussion

The preceding case details a previous relatively healthy 27-year old
man who suffered a lightning injury. He presented with confusion
and cutaneous burns, and developed rhabdomyolysis and cardiogenic
pulmonary edema. Both of these insults resolved after
administration of supportive measures. His 12-lead electrocardiogram
demonstrated diffuse T-wave inversion, late transition shift and long
QT interval, all of which were resolving or showing signs of resolution
at the time of discharge.

Lightning is responsible for more fatalities each year on average than
hurricanes and tornadoes combined. Only about 10% of lightning strike
victims are killed; 90% survive. It is currently estimated that
lightning causes 50 to 300 deaths per year in North America with four
to five times as many victims suffering non-lethal injuries leading to
severe and permanent disability [2]. Early recognition of lightning
injury syndromes and anticipation of complications may help us improve
outcomes for these patients. Among the most dramatic complications of
lightning injury are those associated with the cardiovascular system.
The cardiac complications associated with lightning injury are
widespread range in severity from benign ECG changes to death (Table 1).

Lightning injuries can occur from a direct strike, contact with a
struck object or splash off of another object, as a result of ground
currents or as blunt trauma from the lightning shockwave. Lightning is
different from conventional electrical injuries in that it delivers a
massive unidirectional impulse of current [2]. Multiple mechanisms have
been proposed to explain the cardiovascular manifestations of lightning
injury. These include the induction of coronary artery spasm,
catecholamine-mediated effects, direct thermal damage, ischemia
secondary to arrhythmia and coronary artery ischemia as part of a
generalized vascular injury [3].

Rhythm
disturbances

Cardiac rate and rhythm can be affected both directly and indirectly as
a result of lightning injury. Electrical and mechanical trauma
can have a direct effect, while autonomic stimulation and excessive
catecholamine release may act indirectly. The direct current of a
lightning strike can cause cardiac depolarization and asystole [4].
Reports have been made of atrial arrhythmias, specifically atrial
fibrillation as well as ventricular arrhythmias following lightning
strike, including occurring in previously healthy hearts.
As a general rule, these have tended to revert spontaneously to sinus
rhythm over a period of days [5].

Sudden Cardiac
Death

A common cause of fatality in lightning injury is sudden cardiac death
(SCD). Kondur et al. reported the case of a 75 year old man with an
implanted cardioverter defibrillator (ICD) for primary prophylaxis of
sudden death who was struck by lightning. His device-stored
electrograms revealed ventricular fibrillation that was appropriately
treated by a single ICD shock. [7]. The sudden incidence of
ventricular fibrillation may be most likely to occur with an indirect
lightning strike to an object or the ground near the person, whereas a
passage of direct current through the individual may be more likely to
result in asystole [1].

ECG Changes
Including Long QT

A series of ECG changes have been shown as a result of lightning
injury. These include specific and non-specific ST-segment changes,
transient T-wave inversions, as well as lengthening of the QT interval
and alterations in R-wave progression or late transition shift. Changes
have also been seen that are consistent with ischemia, pericardial
effusion, contusion and changes in repolarization. Palmer
reported a case of a previously healthy patient who developed transient
prolongation of the QTc interval after being struck by lightning,
becoming as long as 680 ms two days after admission and returning back
to normal (QTc=410 s) over the course of a month [6].

Our patient developed a QTc of 500 ms, which normalized to 464 ms over
the course of his admission. Such a change in repolarization could be a
direct result of cellular injury. [6] These cases suggest that QT
interval prolongation could act as a substrate for previously mentioned
ventricular arrhythmias. These findings highlight the importance for
ECG monitoring in the seemingly-stable lightning-injured patient.

Myocardial
Contusion

Lightning strike can result in direct mechanical injury to the
myocardium. This is often reflected biochemically with an increase in
creatinine kinase and troponins. As was the case with our
patient, a number of patients after lightning strike have been shown to
develop a clinical syndrome of hemodynamic deterioration and
cardiogenic shock in the setting of systolic and diastolic dysfunction
as demonstrated by echocardiography. Typically, these patients recover
spontaneously after treatment with supportive measures, as did our
patient. These abnormalities are consistent with stunned
myocardium or cardiac contusion. The exact mechanism of abnormal
contractility in the absence of direct electrofulguration is unknown
but may be explained by release of oxygen free radicals, proteolysis of
the contractile apparatus, and cytosolic overload of intracellular
calcium, followed by reduced myofilament sensitivity to calcium
[6] .

In the case of our patient, he developed wall motion abnormalities with
akinesis of some segments as demonstrated by echocardiography. Symptoms
of heart failure were evident and there was a rise in biomarkers.
It is unclear in his case what contributions to his clinical condition
may have come from myocardial ischemia, cardiac contusion and volume
overload secondary to renal failure (due to rhabdomyolysis). However,
the spontaneous recovery is suggestive of a transient mechanism, such
as contusion.

Myocardial
Ischemia

Myocardial infarction and ischemia have been reported as a consequence
of lightning injury in the absence of any thromboembolic coronary
occlusion or vasoconstriction [9]. Our patient developed diffuse T-wave
inversion and a rise in biochemical markers of myocardial injury after
lightning strike and cardiogenic pulmonary edema that could represent a
manifestation of ischemia. In this setting, the infarction could result
from direct tissue damage from lightning strike (contusion) or
lightning-induced vasospasm.

Takotsubo
Cardiomyopathy

Multiple case reports have emerged in the literature of development of
Takostubo syndrome following lightning injury in previously healthy
patients. This syndrome is characterized by transient apical and
mid-left ventricle wall akinesis, may be accompanied with symptoms of
heart failure and is usually self-resolving. Pathogenetic mechanisms
that have been put forward to explain the development of this syndrome
in the setting of lightning injury include a specific localized
contusion or a consequence of vasospasm of the left anterior descending
coronary artery [3]. In our patient, wall motion abnormalities were
seen, but they were not compatible with Takostubo-type picture and they
were better explained as a simple localized contusion.

Conclusions

Lightning injury is a rare but potentially devastating condition.
Patients who are struck by lightning can incur a range of
cardiovascular complications. Evaluation of these patients should
include a minimum of a detailed history and physical examination,
12-lead ECG and drawing of baseline troponins. Prolonged
electrocardiographical monitoring (for monitoring of ventricular
arrhythmias) and assessment for signs and symptoms of hemodynamic
compromise may be warranted.